A reduction in cardiomyocyte numbers owing to decreased cell division might contribute to the cardiac complications seen in adult patients with tetralogy of Fallot, according to a new study. Analysis of heart tissue from infants with tetralogy of Fallot with pulmonary stenosis showed a higher percentage of binucleated cardiomyocytes, a trait linked to cytokinesis failure, than in normal hearts. Assays in mouse models revealed that cytokinesis failure in cardiomyocytes was associated with low expression of Ect2, mediated by β-adrenergic receptor (β-AR) signalling. Deficiency of β-ARs in neonatal mice or treatment with the β-blocker propranolol during the neonatal phase increased Ect2 expression and decreased cardiomyocyte binucleation, and led to increased cardiomyocyte numbers, improved cardiac function and attenuated remodelling after myocardial infarction in the adult. These findings suggest that treatment with β-blockers early after birth might rescue cytokinesis defects and prevent heart dysfunction in adulthood.
Liu, H. et al. Control of cytokinesis by β-adrenergic receptors indicates an approach for regulating cardiomyocyte endowment. Sci. Transl Med. 11, eaaw6419 (2019)
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Fernández-Ruiz, I. β-Blockers rescue cardiomyocyte division defects. Nat Rev Cardiol 17, 6 (2020). https://doi.org/10.1038/s41569-019-0302-2